The research proposed here will investigate the postnatal development of the retino-geniculo-cortical pathway in the cat. Four sets of experiments are described: (1) In normal and visually deprived cats, the structural development of circuits in the dorsal lateral geniculate nucleus (LGN) and primary visual cortex (area 17) that are thought to use gamma-aminobutyric acid (GABA) as a neurotransmitter will be studied with light and electron microscopic immunocytochemistry, using specific antibodies made against GABA. (2) The effect of substituting electrical stimulation for retinal ganglion cell (RGC) action potentials on the morphological development of retinogeniculate synapses will be investigated by rearing cats with intraocular injection of tetrodotoxin (TTX), to abolish RGC action potentials, while stimulating the optic tract with implanted electrodes. In addition, the development of GABA-positive neurons and terminals in the LGN and area 17 will also be studies in TTX-injected cats using light and electron microscopic immunocytochemistry. (3) The morphology of physiologically classified retinal ganglion cells in adult cats that received a large lesion of visual cortex (areas 17, 18, and 19) at birth will be determined by direct intracellular labeling of single ganglion cells with horseradish peroxidase (HRP). (4) The synaptic organization of normal and deprived geniculocortical axons will be clarified by combining electron microscopy with the intracellular injection of HRP into physiologically identified geniculocortical fibers. The long-term objective of this research is to further our understanding of the postnatal development of the visual system under normal and abnormal conditions. Of particular interest is: (a) the role played by patterned impulse activity in the morphological development of the retino-geniculo-cortical pathway; and (b) the factors that permit compensatory reorganization in the central visual pathway after early lesions. It is intended that this work will shed light on the mechanisms that contribute to the effects of amblyopia or the sequelae that result from damage to central visual structures.